Interestingly, besides producing rearrangements and CNA of oncogenes/oncosuppressors recurrently involved in T-ALL, such as RPL22, TCF7, IKZF1, EZH2, CDKN2AB, ETV6, CDKN1B, TP53, and rearrangement of the HOXA locus, our study provided evidence that it also generated new putative leukemogenic events, broadening the spectrum of oncogenic lesions linked to T-ALL pathogenesis/progression. The gene discussed is TP53; the disease is acute lymphoblastic leukemia.